international
R E V I E W
PRESSURE ULCER PREVENTION
pressure, shear, friction and
microclimate in context
a consensus document
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international
R E V I E W
Managing Editor:
Lisa MacGregor
Expert working group
Editor, wounds
international:
Suzie Calne
Mona Baharestani, Wound Care Specialist/Education & Research, James H Quillen Veterans Affairs
Medical Center, Johnson City, Tennessee, USA; and Clinical Associate Professor, Quillen College of
Medicine, East Tennessee State University, Johnson City, Tennessee, USA
PUBLISHER:
Kathy Day
Joyce Black, Associate Professor, University of Nebraska Medical Center, College of Nursing, Omaha,
Nebraska, USA
PRODUCTION:
Alison Pugh
Keryln Carville, Associate Professor Domiciliary Nursing, Silver Chain Nursing Association & Curtin
University of Technology, Osborne Park, Western Australia
PRINTED BY:
Printwells, UK
Michael Clark, Independent Consultant, Cardiff, UK
PUBLISHED BY:
Wounds International
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London SE1 9PG, UK
Tel: + 44 (0)20 7627 1510
Fax: +44 (0)20 7627 1570
info@woundsinternational.com
www.woundsinternational.com
© Wounds International 2010
Janet Cuddigan, Associate Professor, Chair, Adult Health and Illness Department, College of Nursing,
University of Nebraska Medical Center, Omaha, Nebraska, USA
Carol Dealey, Senior Research Fellow, University Hospitals Birmingham NHS Foundation Trust and
University of Birmingham, Queen Elizabeth Hospital, Birmingham, UK
Tom Defloor, Full Professor, Unit Nursing Science, Department of Public Health, Ghent University,
Belgium
Amit Gefen, Associate Professor, Department of Biomedical Engineering, The Iby and Aladar
Fleischman Faculty of Engineering, Tel Aviv University, Israel
Keith Harding, Professor of Rehabilitation Medicine (Wound Healing), Head of Department of
Dermatology and Wound Healing, Cardiff University, Cardiff, UK
Nils Lahmann, Associate Professor, Department of Nursing Science, Charité Universitätsmedizin
Berlin, Berlin, Germany
Maarten Lubbers, Surgeon, Department of Surgery, Academic Medical Center, University of
Amsterdam, The Netherlands
Supported by an unrestricted
educational grant from KCI.
Courtney Lyder, Dean and Professor, School of Nursing, Assistant Director for Academic Nursing,
Ronald Reagan UCLA Medical Center, University of California, Los Angeles, USA
Takehiko Ohura, Chair, Pressure Ulcer and Wound Healing Research Center (Kojin-kai), Sapporo,
Japan
Heather L Orsted, Director - CAWC Institute of Wound Management and Prevention and Clinical and
Educational Consultant, Canadian Association of Wound Care, Calgary, Alberta, Canada
The views expressed are those
of the authors and do not
necessarily reflect those of KCI.
How to cite this document:
International review. Pressure
ulcer prevention: pressure, shear,
friction and microclimate in
context. A consensus document.
London: Wounds International,
2010.
Vinoth K Ranganathan, Program Manager, Department of Physical Medicine and Rehabilitation,
Cleveland Clinic, Cleveland, Ohio, USA
Steven I Reger, Director Emeritus, Rehabilitation Technology, Department of Physical Medicine and
Rehabilitation, Cleveland Clinic, Cleveland, Ohio, USA
Marco Romanelli, Consultant Dermatologist, Wound Research Unit, Department of Dermatology,
University of Pisa, Italy
Hiromi Sanada, Wound, Ostomy and Continence Nurse, Department of Gerontological Nursing/
Wound Care Management, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
Makoto Takahashi, Associate Professor, Biomedical Systems Engineering, Bioengineering and
Bioinformatics, Graduate School of Information Science and Technology, Hokkaido University, Sapporo,
Japan
Development and consensus process
The development of this document involved a process of text review by the expert working group and
revision by the authors. It culminated in consensus as indicated by sign off from each working group
member and author.
KCI Extrinsic Factors.indd 2
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Pressure, shear, friction and
microclimate in context
HL Orsted, T Ohura, K Harding
The overall goal of clinical care is to restore
or maintain health. Unfortunately, however,
iatrogenic injuries sometimes occur. Although
not all pressure ulcers are iatrogenic, most are
preventable. Pressure ulcers are one of the
most frequently reported iatrogenic injuries in
developed countries. Inappropriate care methods,
such as leaving vulnerable patients in potentially
damaging positions for long periods of time, or
massaging reddened areas of skin, often remain
in practice long after evidence has shown them to
be harmful or ineffective. Education is critical in
ensuring that all members of a clinical team act
to prevent and treat pressure ulcers according to
the best evidence available.
The most recent definition of pressure ulcers,
which has been produced by an international
collaboration of the National Pressure Ulcer
Advisory Panel (NPUAP) and the European
Pressure Ulcer Advisory Panel (EPUAP),
highlights current understanding of the role of
extrinsic factors in the development of pressure
ulcers1,2 (Box 1). Pressure, which is often related
to decreased mobility, has long been viewed as
the most important extrinsic factor in pressure
ulcer development. However, recent and ongoing
research is revealing that shear, friction and
microclimate also have important roles, and that
there are significant and complex relationships
between all of the extrinsic factors. For example,
pressure and shear are closely linked, friction
has a role in the development of shear, and
microclimate influences the susceptibility of skin
and soft tissues to the effects of pressure, shear
and friction.
The concepts involved in understanding
pressure, shear, friction and microclimate and
their synergistic actions in the formation of
pressure ulcers are complex. Consequently,
the expert working group involved in producing
Pressure ulcer prevention: prevalence and incidence
in context3 proposed a new document to aid
understanding of these extrinsic factors. The
expert working group decided that, even though
pressure, shear, friction and microclimate are
inextricably inter-related, this new project would
tackle each extrinsic factor individually with the
aim of building understanding of the physics
involved. This understanding should enable
clinicians to better comprehend developments
in the field and, most importantly, will underpin
effective and consistent implementation of
pressure ulcer prevention protocols.
The three papers – Pressure in context, Shear
and friction in context, and Microclimate in context
– follow a similar structure. They start by
defining the relevant extrinsic factors and how
individually they contribute to the aetiology
of pressure ulcers. The relationships between
the factors are explained and emphasised, and
the evidence for the role of the factors in the
development of pressure ulcers is discussed.
The latter sections of the three papers describe
how patients at risk from each extrinsic factor
can be identified. The papers then explain
the types of and rationale for the clinical
interventions that aim to prevent or ameliorate
the adverse effects of each of the extrinsic
factors discussed. It should be noted that,
although the document covers many major
facets of pressure ulcer prevention, discussion
of comprehensive prevention protocols is
beyond its scope.
Much research remains to be undertaken to
further develop our understanding of the intrinsic
and extrinsic causes of pressure ulcers. But as
this document shows, there are some important
underlying principles for preventing pressure
ulcers resulting from the extrinsic factors of
pressure, shear, friction and microclimate. All
clinicians should understand these principles and
implement them in their daily practice.
REFERENCEs
1. National Pressure Ulcer Advisory Panel and European Pressure
Ulcer Advisory Panel. Prevention and treatment of pressure ulcers:
clinical practice guideline. Washington DC: National Pressure
Ulcer Advisory Panel, 2009.
2. European Pressure Ulcer Advisory Panel and National
Pressure Ulcer Advisory Panel. Prevention and treatment of
pressure ulcers: quick reference guide. Washington DC, USA:
National Pressure Ulcer Advisory Panel, 2009. Available
from: www.npuap.org and www.epuap.org (accessed 23
November 2009).
3. International guidelines. Pressure ulcer prevention: prevalence and
incidence in context. A consensus document. London: MEP Ltd,
2009.
BOX 1 New NPUAP/EPUAP definition of pressure ulcers1
"A pressure ulcer is localized injury to the skin and/or underlying tissue, usually over a bony prominence, as
a result of pressure, or pressure in combination with shear. A number of contributing or confounding factors
are also associated with pressure ulcers; the significance of these factors has yet to be elucidated."
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Pressure in context
M Takahashi, J Black, C Dealey, A Gefen
Introduction
Pressure has been recognised as the most
important extrinsic factor involved in the
development of pressure ulcers for many
years. Consequently, it features prominently in
definitions of pressure ulcers, including the recent
definition produced by the National Pressure
Ulcer Advisory Panel (NPUAP) and European
Pressure Ulcer Advisory Panel (EPUAP)1,2.
This paper explains what pressure is, how
pressure contributes to pressure ulcer formation
and how to identify patients at risk of injury
from pressure. It then describes the rationale
and mode of action of interventions that
reduce the magnitude and duration of pressure
and, consequently, the risk of pressure ulcer
development.
Fact File
●● Force is a concept that
is used to describe the
effect on an object by an
external influence. Force
has a direction and a
magnitude.
●● Perpendicular forces
cause pressure.
●● The pressure at the
junction between the
skin and a support
surface is often called
'interface pressure'.
Figure 1 Definition of
pressure
What is pressure?
Pressure is defined as the amount of force
applied perpendicular to a surface per unit area
of application.
A force applied over a small area will produce
greater pressure than the same force applied
over a larger area (Figure 1). The unit of force is
the newton (N). The unit of pressure is newtons
per square metre (N/m2), pascals (Pa) or
millimetres of mercury (mmHg).
In addition to the perpendicular force that is
involved in pressure, forces may be applied parallel
to the skin surface (Figure 2). These are shear
forces and contribute to shear stresses, which are
also measured in terms of force per unit area (see:
Shear and friction in context3, pages 11–18). 'Stress' is
a generic name for effects that are defined in terms
of force per unit area of application.
perpendicular force (N)
Clinical effects of pressure
In alert patients, the effects of continuous
pressure usually signal frequent small body
movements to relieve the load and restore
tissue perfusion5. Patients who are unconscious,
sedated, anaesthetised or paralysed cannot
sense or respond to these signals and do not
move spontaneously. As a result, the skin and
soft tissues can be subjected to prolonged and
unrelieved pressures.
Pathophysiology of pressure damage
Skin that has been subjected to potentially
damaging levels of pressure initially appears
pale from reduced blood flow and inadequate
oxygenation (ischaemia). When the pressure
is relieved, the skin quickly becomes red due
to a physiological response called reactive
hyperaemia. If the ischaemia has been
sufficiently short lived, blood flow and skin
colour will eventually return to normal.
More prolonged ischaemia can cause blood cells
to aggregate and block capillaries, perpetuating
the ischaemia. Capillary walls can also become
damaged, allowing red blood cells and fluid to
Force
area (m2)
Force
Pressure (N/m2) =
What types of internal stresses does pressure
cause?
When pressure is applied to skin, particularly
over a bony prominence, it distorts the skin and
underlying soft tissues. In the model in Figure 3,
the horizontal lines immediately under the bony
prominence become closer together indicating
tissue compression. In other places, particularly
under the bony prominence, the lines are also
elongated, indicating tensile (stretching) and
shear (distorting) stresses. This means that
even when only pressure is applied (ie the force
applied is only perpendicular), tensile and shear
stresses also occur within the tissues near bony
prominences4.
Perpendicular force
Area of
application
Shear
force
Same force, smaller area = higher pressure
Same force, larger area = lower pressure
Units of pressure
1N/m2 = 1Pa = 0.0075mmHg
1 000N/m2 = 1kPa = 7.5mmHg
N/m2 = newtons per square metre; Pa = pascal; mmHg = millimetres of mercury
Shear
force
Figure 2 Forces applied to a surface
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Figure 3 Tissue distortion
due to pressure (adapted
from6)
Bending of the lines in (b)
shows that when external
pressure is applied over a bony
prominence, compressive,
shear (distorting) and tensile
(stretching) stresses occur
(see bold text on page 2).
Fact File
●● Localised pressure is
thought to contribute
to pressure ulcer
development by
deforming skin and soft
tissues, often between
a bony structure and an
external surface (such
as a bed or a chair),
thereby distorting cells,
reducing blood flow and
inducing ischaemia and
necrosis.
●● Although capillary
closing pressure – ie the
pressure which halts
capillary blood flow –
is often quoted to be
32mmHg, it is highly
variable.
Figure 4 Deep tissue injury
(courtesy of J Black)
DTI over the sacral area
acquired during a long surgical
procedure. It has progressed
so that there is now loss of
skin and exposure of necrotic
subcutaneous tissue.
Tissues
}
Bone
Bone
Shear stress
Compression stress
(a)
}
Tensile stress
(b)
Tissues
Surface pressure
leak into the interstitial space. This process results
in the non-blanchable erythema, skin discolouration
and induration that are seen with Category/Stage I
pressure ulcers. Continued ischaemia results in
necrosis of the skin and underlying tissue, and the
superficial and deeper tissue breakdown seen with
higher category/stage pressure ulcers.
High pressure is also known to physically
damage muscle tissue by deforming and
rupturing muscle cells.
Deep tissue injury
The new NPUAP/EPUAP pressure ulcer
classification contains an additional category
for use in the USA: deep tissue injuries1. Clinical
experience suggests that these usually present
with purple skin around 48 hours following a
pressure event, eg being unconscious on the
floor, and become necrotic quickly, even when
care is provided (Figure 4).
What do we know about pressure
and pressure ulcers?
Because the primary mechanism of pressureinduced tissue damage is thought to be blood
flow reduction, papers that discuss pressure
ulcers frequently mention research done in
the 1930s by Landis. This work found that the
pressure in the arteriolar limb of a capillary in
the human finger was on average 32mmHg7.
This value was then mistakenly generalised to
be the pressure required to compress capillaries
to prevent blood flow (the capillary closing
pressure), and the pressure below which
pressure redistributing devices aimed to reduce
interface pressure. However, many following
studies also demonstrated a wide range of
pressure in capillaries at various anatomical
locations, with values dependent on age and
concomitant disease.
Relationship between duration and intensity of
pressure
By the middle of the 20th century, duration
of pressure was suspected to be a factor in
pressure ulcer development8,9, but quantitative
data were missing until Kosiak started to publish
his experiments in 1959. These involved loading
tissues with known pressures for specific
durations. Histological examination was used to
assess tissue viability10,11.
Kosiak reported a relationship between
amount of pressure, duration of application and
the development of tissue damage in canine and
rat experiments10,11. He stated that, "microscopic
pathologic changes were noted in tissues subjected
to as little as 60mmHg for only one hour"10.
Pressure–time curve
In the 1970s, Reswick and Rogers published
guidelines based on human observations that
depicted non-injurious and injurious levels
and lengths of exposure to particular interface
pressures12 (Figure 5, page 4). Although
consistent with Kosiak's work, the curves at
the extremes of the timescale were based on
extrapolation rather than data13,14.
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Fact File
●● The ability of pressure
to cause tissue damage
is related to duration of
application and intensity
(amount) of pressure
applied.
●● Pressure on the skin has
been shown to produce
greater reductions in
blood flow in a deep
artery than in skin
capillaries.
●● Interface pressure
is relatively easy
to measure, but
has limitations as a
predictor of internal
tissue stresses.
●● When pressure is
applied over a bony
prominence, the internal
stresses are highest in
the soft tissues closest
to the bony prominence.
●● Patients at highest risk
from pressure are those
who are unable to move
themselves or to ask to
be moved.
Intolerable duration and
intensity of pressure
Pressure
Figure 5 Proposed
modification to Reswick and
Rogers pressure–time curve
(adapted from1,15-17)
The area above the curves
represents durations and
intensities of pressure that
are likely to result in tissue
damage; the area below the
curves represents durations
and intensities of pressure
that are unlikely to result in
tissue damage.
Tolerable
duration and
intensity of
pressure
Time
Reswick and Rogers original curve
Proposed curve
Recently, it has been proposed that the
Reswick and Rogers curve be modified to
reflect more recent animal studies and clinical
experience that high pressures can cause
pressure damage within a relatively short time,
but that lower pressures can be applied for
long periods without damage occurring1,15-17
(Figure 5).
Pressure and temperature
The effects of pressure may be modulated by
skin temperature. Work by Kokate et al and
Iaizzo et al in pigs concluded that skin and soft
tissue damage due to pressure could be reduced
by localised skin cooling18,19 (see: Microclimate in
context20, pages 19–25).
Physiological effects
In an experiment to measure the effects of
pressure on blood flow in the human forearm,
pressure ranging from 0 to 175mmHg was
applied to the skin. The results showed that
blood flow was affected by pressure on the
skin to a greater extent in a deep artery than
in a skin capillary21. Future investigations
to measure deep tissue blood flow may
contribute to understanding of the ischaemic
factors in the mechanism of pressure ulcer
formation.
How can internal stresses be measured?
Many studies investigating the role of pressure
in the development of pressure ulcers measure
pressure at the skin surface (interface pressure).
Even so, bioengineering work carried out since
the 1980s has indicated that internal tissue
stresses cannot be predicted by means of
interface pressure measurements13,14.
Stresses within tissues measured in an
animal model demonstrated that pressure is
three to five times higher internally near a bony
prominence than the pressure applied to the skin
over the prominence22. Computer modelling has
confirmed that the highest stresses are near the
bony prominence23.
Identifying patients at risk from
pressure
Patients at highest risk from pressure are those
in whom pressure on skin would go unrelieved if
the healthcare staff did not move them in a bed
or chair. Asking the question, "Can the patient
feel pressure and move about or ask others to
move him?" is an important first step. When the
answer to the question is, "No", high risk patients
can be identified quickly by all staff.
General patient assessment will indicate
other factors, eg reduced tissue perfusion or
poor nutrition, which may make a patient more
vulnerable to the effects of pressure. Some of
these factors increase risk by amplifying the
effects of shear and friction, or by reducing skin
and tissue tolerance to pressure (see: Shear and
friction in context3, pages 11–18 and Microclimate in
context20, pages 19–25).
Several tools are available for assessing
overall risk of pressure ulcer development; these
are based on a number of factors, including
pressure24-26. Although there are limitations to
the use of such tools1 and alternative approaches
have been suggested27, risk assessment tools are
highly valued in clinical practice.
Reducing risk from pressure
Best practice care of patients at risk of pressure
ulceration has numerous facets that aim to
ameliorate the effects of intrinsic risk factors
(such as poor nutrition, concomitant disease,
dry skin) and extrinsic factors (such as shear
and friction, or incontinence). (See: Shear and
friction in context3, pages 11–18 and Microclimate in
context20, pages 19–25.)
With respect to pressure, efforts centre on
reducing or removing the pressure applied to
the skin of vulnerable patients. The principles
involved also apply to patients with existing
pressure damage. Patients should avoid sitting
or lying on areas of non-blanchable erythema
or pressure ulcers. If such areas or wounds fail
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to improve or deteriorate, practitioners must
consider whether continued pressure over the
area is contributing to the problem.
Clinical judgement is essential in determining
how best to provide care for patients at risk from
damage by pressure.
Fact File
Interventions intended
to reduce a patient's
risk from the effects of
pressure must:
●● be planned in the
context of other
care and treatment
requirements
●● centre on encouraging
patients to move
independently, patient
repositioning and the
use of support surfaces
●● take into account
all of the patient's
needs, especially
when determining
the frequency of
repositioning and
positions used.
Pressure redistribution
Pressure redistribution can be achieved by
removal of pressure from the affected part of
the body or by reducing pressure by spreading
weight more widely (Figure 6).
Independent movement
Spontaneous movement is the usual mode
of pressure relief for persons with intact
neurological systems. An early study found that
patients who moved spontaneously fewer than
25 times each night were at significantly higher
risk of pressure ulcers than those who moved
more frequently30.
Wherever possible, patients should be
encouraged to move themselves. For patients
who move spontaneously, sometimes no
additional repositioning is needed. Patients
who are reluctant to move, due to actual or
anticipated pain with movement, or because
of the sedative effects of analgesia, need to be
reminded to move.
The impact of making small, frequent
movements has been studied by testing the idea
that nursing staff could move a patient slightly
with each contact, eg by lifting a leg or moving
an arm, to relieve pressure31,32. The studies
suggested that interface pressure was reduced
under the areas moved31, and in a small study a
reduction in the number of pressure ulcers was
observed32. However, caution must be applied:
unless the heels and pelvis are moved, such
body movements do little to reduce pressure
intensities and durations at these critical
locations.
Repositioning
Repositioning should be considered for all those
deemed to be at risk of pressure ulceration1,33.
More mobile patients will be able to reposition
themselves (see above), but others may require
assistance.
Repositioning may not be suitable for all
patients: some patients in a critical condition
may be destabilised by repositioning. However,
this is not always the case even in patients in
poor haemodynamic condition34. Therefore, the
decision to reposition a critically ill patient should
be individualised.
Frequency of repositioning
A systematic review of pressure ulcer prevention
strategies found insufficient evidence to support
a specific repositioning regimen35. The frequency
of repositioning should be based on the patient's
tissue tolerance, level of mobility, general
medical condition and the support surface in
use1. The traditional 2-hourly repositioning
regimen may provide a useful starting point from
which frequency can be adjusted. An effective
repositioning regimen will be indicated by the
absence of persistent erythema over bony
Pressure redistribution
Increased contact area
reduces interface pressure
Patient
repositioning
to increase contact
area
eg 30˚ tilt position
Figure 6 Methods of
pressure redistribution
(adapted from28,29)
Reactive support
surface*
eg foam, gel or
air filled,
air fluidised
Pressure relief
removes pressure from vulnerable area
Patient
repositioning
to remove pressure
from a particular
anatomical location
Active support
surface*
eg alternating
pressure
Lifting body
part clear
eg heel boots
*A reactive support surface has the capability to change its load distribution properties only in response to applied load;
an active support surface is able to change its load distribution properties with or without applied load.
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prominences. If persistent erythema occurs, this
may indicate that more frequent repositioning is
required and that the current support surface is
perhaps not optimal for the patient.
The use of a pressure redistributing support
surface does not eliminate the need for
repositioning. However, it may be possible to
reduce the frequency of repositioning. In one
study, for example, 4-hourly turning on
a viscoelastic foam mattress was associated
with lower incidence of Category/Stage II and
above pressure ulcers when compared with
2- or 3-hourly turning on a standard
mattress33.
For patients sitting in chairs and wheelchairs,
it is advised that repositioning should occur
at a minimum every hour36. Patients confined
to wheelchairs should be taught to reposition
every 15 minutes by doing 'push-ups' off the
wheelchair or by leaning forwards37.
Fact File
Reactive support surfaces,
eg foams, air or gel filled,
and air fluidised, provide
pressure redistribution
through immersion and
envelopment.
Figure 7 Immersion and
envelopment
Immersion
Positions
For patients in bed, positions such as 90°
side-lying or the semi-recumbent position
are best avoided because these increase
pressure over the trochanteric or sacral bony
prominences respectively1. Patients who must
have some head of bed elevation, eg because
of dyspnoea or to prevent aspiration during
tube feeding, should be repositioned more
frequently.
The 30° tilted side-lying position is a method
of placing a patient so that they are tilted
30° along their vertical axis from the supine
position1. This position does not suit all patients,
but may be a useful alternative for some.
Wheelchair dependent patients may benefit
Envelopment
from a tilting wheelchair that helps to offload
pressure from the ischial tuberosities.
PRESSURE REDISTRIBUTING SUPPORT
SURFACES
Pressure redistributing support surfaces
are available in several forms, eg overlays,
mattresses and integrated bed systems.
An overlay is a support surface device placed
on top of an existing mattress. These devices
may elevate the sleeping surface to the level of
the side rails and so the risk of the patient falling
out of bed must be evaluated. Ideally, the bedrail
should be at least 10cm (4 inches) higher than
the surface of the mattress.
Pressure redistributing mattresses can often
be used to replace standard mattresses, allowing
for continued use of the existing bed frame.
An integrated bed system combines a bed
frame and a support surface (usually an alternating
pressure mattress). They are most often used for
extremely high risk patients, for the treatment of
pressure ulcers, and for patients who have had
surgical reconstruction of pressure ulcers with
flaps.
Reactive support surfaces
Two important principles of the mode of pressure
redistribution of reactive support surfaces are
immersion and envelopment.
Immersion refers to the ability of a support
surface to allow a patient to sink into it29
(Figure 7). As the body sinks in, more of the
body comes into contact with the support
surface, redistributing the patient's weight over a
larger area and reducing pressure.
Partial immersion with envelopment
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Figure 8 Hammock effect
The tight cover prevents
immersion and envelopment
of the patient, resulting in
suspension above the support
surface and no pressure
reduction.
Tight cover
Sagging
support
surface
Small contact area; no pressure reduction
Fact File
●● Active support
surfaces – also known
as alternating pressure
systems – redistribute
pressure mainly through
the inflation and
deflation of sections of
the support surface.
●● The precise indications
for and relative efficacy
of the different types
and models of pressure
redistributing support
surfaces in reducing the
incidence of pressure
ulcers remains under
investigation.
Figure 9 Alternating
pressure support surface
The air cells cyclically inflate
and deflate to periodically
remove pressure from soft
tissue.
Immersion is greater on softer surfaces and
also has the potential to be higher on thicker
surfaces. However, if a material is too soft, the
patient may 'bottom out' (ie end up sitting or
lying on the underlying structure of the bed or
chair because the support surface has become
so compressed).
Envelopment refers to how well a support
surface moulds to body contours and
accommodates irregular areas (such as folds in
clothing or bedding)29 (Figure 7).
Recent research has indicated that the degree
of immersion and envelopment of a support
surface can be impaired by increased tension
at the surface of the support, especially when
combined with sagging of the support surface
itself38. For example, a tight cover over a mattress
or seat cushion can create a hammock effect
that prevents the support surface moulding to
contours and produces high pressures over a
small area (Figure 8).
Immersion and envelopment have
important implications for patient mobility and
independence. For example, it requires relatively
little effort to stand from sitting or lying on wood
(which has no immersion and envelopment), but
the same manoeuvre from water requires more
effort because of the high degree of immersion
and envelopment.
Foam
Basic foam mattresses have become common
as the standard mattress for patients in hospitals
and long-term care facilities. Higher specification
foam mattresses (eg those composed of layers
of different densities of foam, or of viscoelastic
foam) are recommended to reduce the incidence
of pressure ulcers in persons at risk39.
Foam degrades and loses it stiffness over
time, thereby losing its ability to conform. When
a foam mattress wears out the patient may
'bottom out'. The life span of any support surface
is influenced by number of hours of use and the
weight applied; a surface used by thin persons
will outlive one used by bariatric patients.
Air or gel filled
Air or gel filled support surfaces comprise air
or gel filled columns or compartments. The
degree of immersion and envelopment provided
depends upon the pressure of the air or gel in the
compartments, the depth of the compartments,
and the 'give' of the surface.
Air filled support surfaces are sometimes
referred to as low air loss surfaces. However, strictly
speaking, low air loss relates to a property of some
support surfaces that allows air to escape from the
cushions to aid management of skin temperature
and moisture (see: Microclimate in context20, pages
19-25).
Air fluidised
Air fluidised support surfaces provide the
greatest immersion and envelopment of any
support surface. Almost two-thirds of the body
can be immersed. An air fluidised support surface
comprises silicone or glass beads that have
pressurised air forced between them. This makes
the beads take on characteristics of a fluid.
Several randomised controlled studies have
shown that healing outcomes for patients with
Category/Stage III and IV pressure ulcers who
are managed on air fluidised support surfaces are
improved in comparison with standard beds, and
foam and other non-fluidised support surfaces40-43.
Alternating cells
Active support surface – alternating
pressure
Alternating pressure support surfaces redistribute
pressure by cyclically inflating and deflating zones
of the surface (Figure 9). As a result they are less
reliant than reactive surfaces on the properties
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Table 1 Uses of pressure redistributing support surfaces
This table is intended to provide a broad overview of the uses of the different types of pressure redistributing support surfaces. The
specifications, quality and usages for individual products may vary. Clinicians should refer to the manufacturer's literature for information
about indications, cautions and contraindications for individual products.
Type of pressure
redistributing support
surface
Patients who may benefit
Notes
Higher specification foam
n
n
Air* or gel filled
n
Patients who are at low to moderate risk
of pressure ulcers due to immobility and
inactivity
n Patients who are very heavy or rigid and
difficult to reposition
n Some air filled low constant pressure surfaces
can be adjusted for patient weight and weight
distribution by adjusting the amount and
pressure of air pumped through
n
Air fluidised
n
Patients with existing pressure ulcers who
cannot be turned off the ulcer or who have
pressure ulcers on two or more turning
surfaces (eg sacrum and trochanter)
n Patients recovering after flap surgery for
pressure ulcer repair
n
n
n
Reactive support surfaces
Patients who are at low to moderate risk
of pressure ulcers due to immobility and
inactivity
Where possible avoid use of plastic products
such as incontinence pads to minimise heat and
moisture retention on the skin
Accidents have occurred if air cells have suddenly
deflated and then reflated, eg following loss of
electrical power; ideally should be used when
generator back up is available
n Gel filled support surfaces may increase skin
moisture
Patients with large open wounds may become
dehydrated because of the large volumes of air
moving through the support surface
n Some patients are not able to tolerate the
sensation of floating or the warmth of the surface
Active support surface
Alternating pressure
Patients who cannot be turned side to side or
do not move body areas
Inflation and deflation can be annoying, especially
for certain patient groups, eg those with dementia
n Patients may feel disturbed by the noise or may
feel cold
*Sometimes air filled support surfaces are called low air loss surfaces. Strictly speaking, however, low air loss relates to a property of some support
surfaces that allows air to escape from the cushions to aid management of skin temperature and moisture (see: Microclimate in context20, pages 19–25).
Fact File
Patients should continue
to be repositioned when on
a support surface for their
comfort and functional
ability, as well as for
pressure relief, unless
medically contraindicated.
of immersion and envelopment to redistribute
pressure. The ideal frequency, duration, amplitude
and rate of inflation and deflation have not been
determined. A draft consensus document has
recently proposed a standardised method for
evaluating active support surfaces44.
Iglesias et al reported that alternating pressure
mattresses were likely to be more cost effective
than alternating pressure overlays45. In addition,
the mean time to develop a pressure ulcer was
more than 10 days longer on the alternating
pressure mattress than on the alternating pressure
overlay45. When alternating pressure mattresses
were compared with viscoelastic foam mattresses,
Vanderwee et al found no significant difference
in the incidence of pressure ulcers46. There was a
tendency for more sacral pressure ulcers in patients
on alternating pressure mattresses in patients
who were identified as being in need of preventive
measures based on the Braden scale46.
A literature review of 15 randomised
controlled trials concluded that when taking
into account methodological issues, alternating
pressure mattresses are likely to be more
effective than standard hospital mattresses in
the prevention of pressure ulcers47.
Support surface selection
Selection of a suitable support surface for
pressure redistribution (Table 1) should not be
based on risk assessment score alone, but should
also take into consideration:
■■ level of mobility within the bed – ie how
much the patient can move when in bed and
whether they are able or need to be able to
get themselves out of bed
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Fact File
Regular observation is
essential in evaluating
the efficacy of pressure
redistribution strategies:
any sign of pressure
damage should prompt reevaluation of the strategies
in place.
■■ patient comfort – some patients find some
■■ gel mattresses have gel throughout them and
support surfaces uncomfortable
■■ need for microclimate management – some
support surfaces assist with managing heat
and moisture directly below the patient (see:
Microclimate in context20, pages 19–25)
■■ care setting – for example, some integrated
bed systems are unsuitable for home settings
because of their weight and the need for an
alternative power source, eg a generator, in
case of loss of electrical power.
that there are no areas where gel has been
moved away
■■ an alternating air mattress is inflating and
deflating properly
■■ a powered device is plugged into a power
supply.
Even so, one study has shown that
reimbursement guidelines, not patient condition,
were most clearly associated with support
surface selection48.
Higher specification foam mattresses (eg
viscoelastic foam mattresses) are suitable for
many at-risk patients, but those at higher risk will
need a powered support surface that is able to
change its load distribution properties.
Bariatric patients may be too heavy for some
pressure redistributing support surfaces and
require versions with extra width or features
designed to accommodate high patient weight.
Additional features of integrated bed
systems may include lateral rotation or
vibration of the support surface to assist
patients who have problems with ventilation
and perfusion. 'Turn assist' is designed to aid
repositioning, examinations and linen changes;
it is not intended for patients to use in turning
themselves.
Observation and re-evaluation
Once pressure redistribution strategies have
been set in place, it is important to assess their
effectiveness. The most important indicator
is the presence or absence of changes in skin
status, especially over the bony prominences.
If there are indications of pressure damage, the
prevention strategies may need to be intensified
and/or modified. Changes in the condition of
patients and their ongoing risk levels should also
be monitored as these may alter the prevention
strategies required.
When a specialised support surface is in use,
carers should check regularly that the device is
working properly and ensure that:
■■ a foam mattress is still 'springing back' to its
original position when pressure is removed
■■ air filled devices are properly inflated
All support surfaces, hospital beds and
integrated bed systems have a finite term of
use, but the exact lifespan is currently unknown.
Healthcare practitioners need to be mindful
of this and when pressure ulcers fail to heal
consider whether a 'worn out' support surface
may be the cause or play a role.
Conclusion
In addition to a direct effect, pressure also
acts indirectly through the generation of shear
stresses to produce pressure ulcers. The ability
of pressure to produce pressure damage in soft
tissues is related to the intensity and duration
of the applied pressure. Patients who are
unable to move or ask to be moved are those
most at risk from pressure. Interventions to
reduce the effect of pressure and reduce the
incidence of pressure ulcers include patient
repositioning and the use of specialised
support surfaces.
Decisions on which support surface to use
can be enhanced through appreciation of how
surfaces work and for which patients each
device is most suitable. However, despite
expert clinical opinion, the choice of support
surface is often made on a financial basis.
Continued research into the effectiveness
of pressure redistributing support systems
in reducing the incidence of pressure
ulcers will guide educational priorities, aid
decision making and help to secure funding
for appropriate surfaces, regardless of care
setting.
References
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November 2009).
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7. Landis EM. Micro-injection studies of capillary blood
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8. Guttmann L. Rehabilitation after injuries to the spinal cord
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9. Husain T. An experimental study of some pressure effects
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10. Kosiak M. Etiology and pathology of ischemic ulcers. Arch
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13. Gefen A. Reswick and Rogers pressure-time curve for
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16. Stekelenburg A, Strijkers GJ, Parusel H, et al. Role of ischemia
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17. Gefen A, van Neirop B, Bader DL, Oomens CW. Straintime cell-death threshold for skeletal muscle in a tissueengineered model system for deep tissue injury. J Biomech
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18. Kokate JY, Leland KJ, Held AM, et al. Temperature-modulated
pressure ulcers: a porcine model. Arch Phys Med Rehabil 1995;
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19. Iaizzo PA, Kveen Gl, Kokate JY, et al. Prevention of pressure
ulcers by focal cooling: histological assessment in a porcine
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20.Clark M, Romanelli M, Reger S, et al. Microclimate in
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21. Shitamichi M, Takahashi M, Ohura T. Study on blood flow
change of the radial artery and skin under pressure and shear
force. Jpn J Press Ulc 2009; 11(3): 350.
22.Le KM, Madsen BL, Barth PW. An in-depth look at pressure
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23.Takahashi M. Pressure ulcer: up-to-date technology. The
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24.Bergstrom, N, Braden B, Laguzza A, Holman V. The Braden
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25.Norton D, McLaren R, Exton-Smith AN. An investigation of
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26.Waterlow J. Pressure sores: a risk assessment card. Nurs
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27. Vanderwee K, Grypdonck M, Defloor T. Non-blanchable
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28.Rithalia S, Kenney L. Mattresses and beds: reducing and
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29.National Pressure Ulcer Advisory Panel. Support Surface
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30.Exton-Smith AN, Sherwin RW. The prevention of pressure
sores: significance of spontaneous bodily movements. Lancet
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31. Brown M, Boosinger J, Black J, Gaspar T. Nursing innovation
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32.Oertwich PA, Kindschuh AM, Bergstrom N.The effects of
small shifts in body weight on blood flow and interface
pressure. Res Nurs Health 1995; 18 (6): 481 -88.
33.Defloor T, De Bacquer D, Grypdonck MH. The effect of
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devices on the incidence of pressure ulcers. Int J Nurs Stud
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34.de Laat E, Schoonhoven L, Grypdonck M, et al. Early
postoperative 30 degrees lateral positioning after coronary
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16(4): 654-61.
35.Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a
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36.Panel for the Prediction and Prevention of Pressure Ulcers
in Adults. Pressure Ulcers in Adults: Prediction and Prevention.
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38.Iizaka S, Nakagami G, Urasaki M, Sanada H. Influence of the
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39.McInnes E, Cullum NA, Bell-Syer SEM, Dumville JC. Support
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40.Allman RM, Walker JM, Hart MK, et al. Air-fluidized beds or
conventional therapy for pressure sores. A randomized trial.
Ann Intern Med 1987; 107(5): 641-48.
41. Jackson BS, Chagares R, Nee N, Freeman K. The effects of a
therapeutic bed on pressure ulcers: an experimental study. J
Enterostomal Ther 1988; 15(6): 220-26.
42.Munro BH, Brown L, Haitman BB. Pressure ulcers: on bed or
another? Geriatr Nurs New York 1989; 10(4): 190-92.
43.Strauss MJ, Gong J Gary BD, et al. The cost of home airfluidized therapy for pressure sores. A randomized controlled
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44.Tissue Viability Society. Laboratory measurement of the
interface pressures applied by active therapy support
surfaces: A consensus document. J Tissue Viabil 2010;
published online 25 January 2010.
45.Iglesias C, Nixon J, Cranny G, et al. Pressure relieving support
surfaces (PRESSURE) trial: cost effectiveness analysis. BMJ
2006; 332: 1416.
46.Vanderwee K, Grypdonck MH, Defloor T. Effectiveness
of alternating pressure air mattress for the prevention of
pressure ulcers. Age Aging 2005; 34(3): 261-67.
47. Vanderwee K, Grypdonck M, Defloor T. Alternating pressure
air mattresses as prevention for pressure ulcers: a literature
review. Int J Nurs Stud 2008; 45(5): 784-801.
48.Baumgarten M, Margolis D, Orwig D, et al. Use of pressureredistributing support surfaces among elderly hip fracture
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Shear and friction in context
SI Reger, VK Ranganathan, HL Orsted, T Ohura, A Gefen
Fact File
●● Shear stresses arise
from forces applied
tangentially to a surface
and cause deformation
of the object involved.
●● Shear stresses usually
occur in combination
with pressure.
●● Friction force occurs
when two objects rub
against each other.
●● Friction is not a direct
cause of pressure ulcers,
but is involved in the
development of shear
stresses in skin and in
deeper tissue layers.
Introduction
Shear and friction are often mentioned alongside
pressure in the context of pressure ulcers.
For example, the most recent definition of
pressure ulcers, produced by an international
collaboration of the National Pressure Ulcer
Advisory Panel (NPUAP) and European Pressure
Ulcer Advisory Panel (EPUAP), emphasises
the role of pressure and states that shear can
be involved in combination with pressure in
the development of pressure ulcers1. The same
collaboration also cites shear in the context of
deep tissue injury, which is defined as "due to
damage to underlying soft tissues from pressure
and/or shear"1.
Although disputed as a direct cause of
pressure ulcers, friction is considered in this
paper because of its close association with shear.
Pressure and shear are also intimately linked:
pressure on soft tissues, especially when over
a bony prominence, will cause some degree of
shear through tissue distortion2,3.
The first part of this paper clearly defines
shear and friction and discusses the role of each
in pressure ulcer development. The second part
of the paper examines how to recognise patients
at risk of skin and soft tissue injury due to shear
and friction. It then discusses the actions that
can be taken to avoid or minimise shear and
friction and so complement other measures
to reduce the overall risk of pressure ulcer
development.
Definitions
The terminology surrounding shear can be
confusing: 'shear' is often used to abbreviate
the different terms 'shear stress' and 'shear
force'. In addition, shear and friction are often
mentioned together in the context of pressure
ulcer aetiology, and sometimes, inaccurately, the
terms are used interchangeably.
What is friction?
Friction is defined as the force that resists the
relative motion of two objects that are touching,
and is measured in newtons (N). However, the
term 'friction' is also frequently used to mean the
action of one object rubbing against the other
(see: page 14 and Box 2 for more detail).
What causes shear stresses?
Gravity produces a force that pulls a patient onto
the surface they are resting on. The opposing
force produced by the surface can be divided into
two components:
■■ a perpendicular component – which results in
pressure
■■ a tangential component – which results in
shear stresses (Figure 2, page 12).
Box 1 Defining shear stress
Shear stress = Tangential force applied (N)
(pascals or Area of application of force (m2)
N/m2)
1Pa = 1N/m2
Figure 1 Shear stress
Object before
application of
external force
What is shear?
Shear stress results from the application of
a force parallel (tangential) to the surface of
an object while the base of the object stays
stationary. (Note: Pressure is the result of a force
that is applied perpendicular (at a right angle) to
the surface of an object (see: Pressure in context3,
pages 2–10).)
Shear stress causes the object to change shape
(deform) (Figure 1). The amount of deformation
caused by shear stress is quantified as shear strain.
In common with pressure, shear stress is
calculated in terms of the force applied over the
area to which it is applied (Box 1) (see: page
14 and Box 2 for more detail). Shear stress is
expressed in the same units as pressure: most
commonly as pascals (Pa), or sometimes as
newtons/square metre (N/m2).
Tangential
(parallel)
force
Application of
tangential force
produces
deformation and
shear stress
Angle produced by
deformation = shear strain
1kPa = 1000N/m2
Definitions of shear stress:
●● "An action or stress resulting from applied
forces which causes or tends to cause two
contiguous internal parts of the body to
deform in the transverse plane (ie shear
strain)."4
●● "The force per unit area exerted parallel to the
plane of interest."5
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Fact File
Shear stresses are caused
by:
●● friction, eg when sliding
down a bed
●● uneven pressure
distribution, eg over a
bony prominence.
Figure 2 Pressure and shear
applied to the sacral area of
a partially reclined patient
(adapted from9)
Friction contributes to the development of
shear stresses by tending to keep the skin in
place against the support surface while the rest
of the patient's body moves towards the foot
of the bed or the edge of the seat. The relative
movement of the skin and underlying tissues
causes shear stresses to develop in the soft
tissues overlying bony prominences such as the
sacrum.
The angle of the back support of a bed, or
the angle of the backrest of a seat or wheelchair,
strongly influences the level of shear stresses
in tissues6,7. All angles between an erect
sitting posture and horizontal lying will cause
shear stresses due to the body's tendency to
slide downwards along the slope. Lying with
the backrest at an angle of 45° will cause a
particularly high combination of shear stresses
and pressure at the buttocks and sacral area
because, in this posture, the weight of the upper
body divides equally into perpendicular and
tangential forces6,8.
Shear stresses in tissues may also be caused
by localised pressure applied to a skin surface.
The application of pressure causes compression
of the tissues, and by doing so distorts adjacent
tissues (Figure 3). This is sometimes known as
pinch shear. Steep pressure gradients, ie large
changes in pressure across a small surface area,
are likely to produce high pinch shear.
Tangential component
Perpendicular component
Pressure =
Force produced as a result of gravity
pulling the patient down into the bed
perpendicular component of force
contact area
Shear stress =
tangential component of force
contact area
Bone
Shear stress
(pinch shear)
}
Tensile stress
Compression stress
Tissues
Surface pressure
Figure 3 Uneven pressure distribution as a cause of
shear stresses (adapted from10)
How do shear stresses contribute to
pressure ulcer development?
Shear stresses are thought to act in conjunction
with pressure to produce the damage and
ischaemia of the skin and deeper tissues that
results in pressure ulcers. The mechanisms
involved include distortion of tissues, pinching
and occlusion of capillaries crossing tissue
planes, reductions in blood flow, and physical
disruption of tissues or blood vessels.
Tissue distortion
In layered objects, eg body tissues, shear
stresses can cause one layer to move relative
to another (Figure 4). When shear stresses are
applied to tissues, the amount of movement
between the layers in the tissues – ie the degree
of potential for producing blood vessel occlusion
and physical disruption of tissues – is affected
by the looseness of the connective tissue fibres
between the layers11 and the relative stiffnesses
of the tissue layers.
In aged skin, skin elasticity and skin
turgor tend to be reduced. As a result, more
pronounced skin tissue displacements can take
place in skin and subdermal layers when external
forces are applied12.
Differences in the stiffnesses of distinct tissue
layers mean that they deform to varying extents
when an external force is applied. Stiffer tissues
deform to a lesser extent than materials of
lower stiffness. Table 1 shows that the greatest
difference in stiffness of adjacent tissues, ie the
greatest potential for shear stresses to occur,
is between the bone and muscle13-15, but that
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Figure 4 Effect of shear
stress on body tissue layers
(courtesy of T Ohura)
When shear force is applied,
friction between the skin and
support surface tends to hold
the skin in place while deeper
tissues are displaced. The
amount of displacement, ie
shear strain, is greater in the
vicinity of the bone than in the
superficial tissue layers.
Bone
Muscle
Adipose tissue
Skin
Support surface
potential for shear stresses also occurs between
muscle and adipose tissue, and between adipose
tissue and skin.
This helps to explain why pressure ulcers
frequently develop over bony prominences,
where interface pressures also tend to be
highest16,17. Patients with prominent bones are
particularly prone to shear stresses and pressure,
and slender body types tend to have higher shear
stresses and pressure at the coccyx and sacrum
than do obese body types18.
Fact File
●● Shear stresses act in
conjunction with, and
amplify the effects of,
pressure to produce the
ischaemia and tissue
damage that may result
in the development of
pressure ulcers.
●● Although shear stresses
can be measured on
the skin surface and
computer modelling
is helpful, there
remains a need for the
development of devices
that directly measure
shear stresses in deeper
tissues, eg muscle and
adipose tissue.
Shear
force
Effects on blood vessels
Shear stresses can reduce or prevent blood flow
through a number of mechanisms:
■■ direct compression and occlusion of blood
vessels (Figure 4)
■■ stretching and narrowing of dermal capillary
beds – when sufficiently high shear stresses are
applied, the internal diameter of the capillaries
becomes inadequate for blood flow19,20
■■ bending and pinching of blood vessels running
perpendicular to the skin surface21.
The capillaries in adipose tissue are also
vulnerable to the effects of shear stresses
because adipose tissue lacks significant tensile
strength (ie it distorts and tears apart easily)22.
Table 1 Relative stiffness of body tissues (based on animal studies)13-15
Body tissue
Stiffness (as indicated by elastic
modulus (kPa))
Bone
20,000,000
Muscle
7
Adipose tissue
0.3
Skin
2–5
Friction between skin and
support surface
Deeper and larger blood vessels may also be
affected by shear stresses. The blood supply for
skin and subcutaneous tissues can be traced
back to arteries that arise below the deep fascia
and muscle. These arteries – known as perforator
vessels – tend to run up perpendicular to the
surface and to supply considerable areas. Their
perpendicular route makes them particularly
prone to shear stresses, and may explain the
observation that some larger sacral pressure
ulcers tend to follow the supply pattern of
specific blood vessels.
Pressure and shear stresses usually work in
tandem to reduce blood flow. Biomechanical
modelling has demonstrated that shear stresses
applied in addition to pressure cause greater
obstruction and distortion of capillaries in
skeletal muscle around bony prominences than
does pressure alone20. At sufficiently high levels
of shear stresses, only half as much pressure is
required to produce blood vessel occlusion as
when little shear stress is present23. Conversely,
if shear stresses are reduced, tissues can tolerate
higher pressures without blood flow occlusion20.
Measuring shear stresses
Several devices are available for measuring shear
stresses at skin surface interfaces18,24,25; some
devices also simultaneously measure interface
pressure15,26. Internal shear stresses are difficult
to measure directly, but have been estimated
using computer modelling27 and using computer
modelling in combination with magnetic
resonance imaging (MRI)16,17.
What affects friction?
Friction force at the patient-support surface
interface is dependent on the perpendicular
force and the coefficient of friction of the skin
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and the contact surface (Box 2). The higher the
perpendicular force, the higher the friction force.
Similarly, the higher the coefficient of friction, the
higher the friction force and the greater the force
required to make the patient move in relation to
the support surface.
The coefficient of friction of textiles or other
materials against skin is mainly influenced by:
■■ the nature of the textile – eg rougher textiles
produce higher coefficients of friction
■■ skin moisture content and surface wetness –
these increase the coefficient of friction and
are particularly relevant in the clinical context
where skin may be damp from perspiration or
because of incontinence (see: Microclimate in
context28, pages 19–25)
■■ ambient humidity – high ambient humidity
may increase skin moisture content or induce
sweating and therefore increase coefficient of
friction (see above)29.
Fact File
●● The magnitude
of friction force is
dependent on the
perpendicular force and
a characteristic of the
interaction of the two
objects known as the
coefficient of friction.
●● Moist skin has a higher
coefficient of friction
than does dry skin, and
is therefore more likely
to be exposed to higher
levels of friction and
shear stresses.
●● Much research is
required to fully unravel
how shear stresses
cause tissue damage,
the effect of the
frequency and/or speed
of postural changes
on shear stresses, and
which patients are at
greatest risk of injury
from shear stresses4.
●● Many of the
interventions aimed
at reducing shear
stresses and friction
revolve around
attempts by healthcare
professionals, carers
or patients themselves
to move or reposition
patients, as it is during
such manoeuvres that
there is increased risk of
shear stress and friction
occurring.
A study looking at the interaction between
skin and a polyester/cotton textile confirmed
that as skin moisture increased, the coefficient of
friction also increased29. The same study found
that the coefficient of friction for wet fabric on
skin was more than double the value for dry
fabric on skin29.
How might friction contribute to
pressure ulcer development?
The significance of friction in the context of
pressure ulcers lies mainly in its contribution
to the production of shear stresses. When the
tangential force applied by friction at the skin
surface is larger than the perpendicular force
(pressure), or when a small amount of pressure
with a large tangential force is applied to the skin,
abrasions, superficial ulceration or blistering may
occur. If the skin is already irritated or inflamed,
eg by maceration, incontinence-associated
dermatitis or infection, superficial damage due to
friction will occur more easily. Friction applied to
the skin surface can also cause shear stresses in
deeper tissue layers such as muscle.
Measuring friction
Experiments related to the measurement of
friction usually determine the coefficient of
friction of the materials being examined. A
standardised method used commonly calculates
the coefficient of friction between a block
Box 2 Friction
Friction force opposes externally applied forces;
movement of one surface against another will
only occur when the applied force is greater than
the friction force. The friction force produced
by two surfaces in contact is dependent on
the perpendicular force (related to the weight
of the object) and the coefficient of friction.
The coefficient of friction is a value that is
dependent on the properties of the two objects
that are in contact.
Applied force
pushing upper
material
Perpendicular
force
Friction force (N) =
perpendicular force x coefficient of friction
Definitions from the Support Surface Standards
Initiative5:
■ Friction – "The resistance to motion in a parallel
direction relative to the common boundary of two
surfaces."
■ Coefficient of friction – "A measurement of the
amount of friction existing between two surfaces."
of metal and a fabric30. This standardisation
should allow for comparison between textiles
to be made easily. However, differences in
equipment and methods of measurement used
in those studies that have been conducted make
comparisons of results difficult29-33, and the role
of textiles in the prevention and formation of
pressure ulcers is understudied34,35.
Management of shear stresses and
friction
Alongside pressure redistribution, patient
repositioning and mobilisation, strategies
to reduce shear stresses and friction form
an important part of best clinical practice to
reduce patients' overall risk of pressure ulcer
development.
A number of guidelines for the prevention
of pressure ulcers have developed
recommendations to assist with decision making
about appropriate health care. These include the
recent guidelines produced by the NPUAP and
EPUAP1 and those produced by the Registered
Nurses' Association of Ontario36. Decisions for
care will require clinical judgement based on
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patient risk, availability of resources, patient
comfort and wishes, and other treatment or care
needs.
The principles involved in minimising the
effects of shear stresses and friction include:
■■ decreasing tangential forces – eg during lying,
by minimising head of bed elevation, and
during sitting, by avoiding sliding downwards/
forwards7
■■ avoiding actions that induce tissue distortion
– eg avoiding sliding or dragging, by ensuring
that patients are positioned in a way that does
not allow them to slip easily and by ensuring
that body tissues are not dragged upon
during repositioning or left distorted following
repositioning
■■ increasing contact area with support
surfaces – this spreads the perpendicular and
tangential loads and friction force over a larger
area, reducing the localised pressure and
shear stresses11.
The use of lower coefficient of friction textiles
to cover support surfaces will reduce friction
force and shear stresses. However, a balance is
required: if the coefficient of friction is too low,
the patient may slide around on the support
surface and be difficult to place in a stable
position.
Fact File
Patients at particular risk
from shear and friction are
those:
●● at risk of pressure
damage
●● who require head of bed
elevation
●● with damp or damaged
skin
●● who are difficult to
reposition.
Figure 5 Friction damage
(courtesy of H Orsted)
This patient has superficial
abrasions related to sheet
burn and scratch trauma from
a caregiver's ring.
Clinical practice steps
Best clinical practice begins with identification
of those at risk and ends with an evaluation
of the impact of implementation, ie effect on
incidence and prevalence of pressure ulcers.
Clinical recommendations from the recent
NPUAP and EPUAP guidelines1 that particularly
relate to shear stress and friction are reviewed
in the practice steps below. The majority of
these recommendations are classified as having
'strength of evidence = C', meaning that they are
supported by indirect evidence and/or expert
opinion1.
Step 1: Identify those at risk from shear
stresses and friction
■■ Establish a risk assessment policy in all
health care settings1.
■■ Consider the potential impact of following
factors on an individual’s risk of pressure
ulcer development: friction and shear,
sensory perception, general health status
and body temperature1.
Box 3 lists the types of patients at increased
risk of shear stresses and friction.
Box 3 Patients at risk of shear stresses and
friction
Patients that:
●● must have head of bed elevation because
of difficulty breathing or the use of medical
devices such as ventilators or tube feeding
equipment
●● are difficult to reposition without some sliding
across bed sheets or support surface
●● slip or slide from a position that they have
been placed in when in a bed, chair or
wheelchair – eg patients who are unable to or
find it difficult to position themselves because
they are immobile, have sensory loss or are
physiologically unstable
●● are too weak or too unstable to be able to
reposition themselves effectively without
dragging across sheets or support surfaces
●● have moist, wet or macerated skin where the
skin touches a support surface or another skin
surface (skin folds/pannus) – eg due to sweat,
incontinence or leaking dressings
●● are exposed to high pressures, especially over
bony prominences – eg very thin patients
●● are obese – risk may be increased because of
immobility and difficulties with transfers or
repositioning, increased sweating and poor
perfusion of adipose tissue37
●● have decreased skin elasticity and/or turgor –
eg due to ageing or dehydration
●● have fragile skin – eg due to steroid or
anticoagulant use, scar tissue over a healed
pressure ulcer, inflammation or oedema
●● have signs of existing skin friction damage – eg
superficial abrasions or blistering on areas in
contact with support surfaces (Figure 5)
●● have a current or healed pressure ulcer
●● have developed undermining in an existing
pressure ulcer – this may signify that shear
stresses are being applied; the undermining
in such cases will be towards the underlying
bony prominence38
●● have an irregularly shaped pressure ulcer39
●● tend to rub their heels on the bed due to
agitation – eg as a result of pain or dementia
●● have dressings that show partial peeling along
one edge – the forces involved may be coming
from the side of the peeling.
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The three most commonly used pressure
ulcer risk scales (Braden, Norton and Waterlow)
all recognise moisture or incontinence as a risk
factor for pressure ulcers40-42. However, only
the Braden scale specifically evaluates friction
and shear; it does so on the basis of the level of
assistance required to move, frequency of sliding
in a bed or chair, and the presence of spasticity,
contractures or agitation that cause friction40.
Step 2: Assess those at risk from shear
stresses and friction
■■ Ensure that a complete skin assessment is
part of the risk assessment screening policy
in place in all health care settings1.
Complete skin assessment will enable
clinicians to determine the presence of existing
pressure ulcers and to look for signs that indicate
that the patient is at risk of shear stresses and
friction (see Step 1).
Although it is very important to distinguish
clinically between pressure ulcers and moisture
lesions such as incontinence-associated
dermatitis43, the presence of moisture lesions
increases the coefficient of friction of skin,
and consequently risk from shear stresses and
friction.
If damage due to shear stresses and friction
has already occurred, determining how shear and
friction were involved may suggest interventions
to prevent further damage. For example, if a
wheelchair user develops damage, analysis of
how transfers are made may reveal that 'drag' is
occurring and suggest interventions that reduce
drag.
Step 3: Provide care for those at risk from
shear stresses and friction
Skin care
■■ Do not vigorously rub skin that is at risk for
pressure ulceration1.
Skin rubbing is an outdated practice that
unfortunately persists in some places. When
clinicians rub already reddened and inflamed
tissues there is a possibility of damage to the
underlying blood vessels and/or to the fragile
skin36,44,45.
If emollients are applied to skin, they should
be applied gently to avoid unnecessary trauma.
Incompletely absorbed emollients that leave a
sticky residue on the skin and may increase the
coefficient of friction should be avoided. There is
anecdotal evidence that application of siliconebased lotions to the skin of patients who have a
lot of drag or resistance during repositioning may
ease friction.
Management of skin moisture to avoid it
becoming damp or macerated is important to
avoid increasing the coefficient of friction of
the skin (see: Microclimate in context28, pages
19–25).
■■ Consider using film dressings to protect body
areas at risk for friction injury or risk of injury
from tape1.
An increasing range of dressing products
(including film dressings) that aim to reduce
shear stresses and friction over vulnerable
areas is under investigation46. Transparent
dressings, eg films, aid monitoring of the
underlying skin. A study using an animal model
found that film dressings produced greater
reductions in shear and pressure than did other
types of dressings26.
Dressing types that have been studied
clinically include a hydrocolloid dressing that has
a low coefficient of friction outer surface. This
dressing was found to reduce shear force when
applied to areas susceptible to shear damage
such as the heel47, and to significantly reduce the
incidence of persistent erythema when placed
over the greater trochanter48. In a more recent
study, application of a soft silicone dressing to
the sacrum in high risk intensive care patients
was associated with a reduction in sacral
pressure ulcer incidence to zero49.
Positioning
■■ Select a posture that is acceptable for the
individual and minimizes the pressure and
shear exerted on the skin and soft tissues1.
■■ Limit head-of-bed elevation to 30 degrees
for an individual on bedrest, unless
contraindicated by medical condition.
Encourage individuals to sleep in a 30 to 40
degree side lying position or flat in bed if not
contraindicated1.
■■ Use transfer aids to restrict friction and
shear. Lift – don't drag – the individual when
repositioning1.
■■ If sitting in bed is necessary, avoid head of bed
elevation or a slouched position that places
pressure and shear on the sacrum and coccyx1.
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The input of specialist advisers on seating
and support surfaces may be required
to ensure that the patient is placed in a
comfortable position that minimises shear
and friction, and avoids head of bed elevation.
Slight knee gatch (elevation of a bend in a
support surface at the level of the knees)
engagement may help to prevent the patient
from sliding down the bed.
The recommendation for limiting head of
bed elevation is based on a study performed
in healthy volunteers. This found that the 30°
semi-Fowler position (which involves 30° head
of bed elevation and 30° elevation of the legs)
produced lower pressure and shear stresses
than did a supine position with 30° head of
bed elevation50. The same study found that a
30° side-lying position gave lower interface
pressure readings than the 90° side-lying
position50.
However, patient positioning needs to
consider all of the patient's needs. For example,
if the patient is being ventilated, critical care
protocols may recommend 30-45° head of bed
elevation.
The risk of friction burns can be reduced
by careful repositioning of patients to avoid
dragging across the support surface cover, and
the use of turning sheets or transfer aids51.
Support surfaces
■■ Provide a support surface that is properly
matched to the individual's needs for
pressure redistribution, shear reduction, and
microclimate control1.
Support surface selection may require
multidisciplinary input. In addition to relief
of pressure and shear stress, support surface
selection should take into account factors such
as ability to manage aspects of microclimate, eg
skin moisture and temperature (see: Microclimate
in context28, pages 19–25).
Following repositioning, some clinicians
advise that the patient is briefly moved away
from the support surface to help release shear
forces that have built up during the manoeuvre.
This also provides an opportunity to check that
the support surface has not become wrinkled
and that the patient's skin is smooth and has not
become distorted.
Shear forces can be reduced during bed
operation when a patient is supine by bending
the knees, and matching the body's bending
points with those of the bed18.
■■ Prevent shear when lateral-rotation features
are used. Assess skin frequently for shear
injury1.
Lateral rotation features of some beds allow
the patient to be turned from side to side through
mechanical movement of the bed. However,
such beds are unable to fully reposition patients
and positioning aids will be required to maintain
good body alignment and to prevent shift within
the bed. Patients should be observed regularly
through several rotations to check for sliding
movement that could cause shear and friction.
Conclusion
Shear stresses – and by association, friction –
are important extrinsic factors involved in the
development, and sometimes persistence, of
pressure ulcers. However, many uncertainties
remain about the role and critical levels for shear
stress and friction in pressure ulcer development.
Even so, a clear understanding of how shear
stresses and friction occur will undoubtedly
assist clinicians in consistent implementation of
aspects of pressure ulcer prevention protocols
designed to minimise shear stresses and avoid
increasing the coefficient of friction of skin.
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pressure ulcer preventive dressings for reducing shear force
on the heel. J Wound Ostomy Continence Nurs 2006; 33(3):
267-72.
48.Nakagami G, Sanada H, Konya C, et al. Evaluation of a new
pressure ulcer preventive dressing containing ceramide 2 with
low frictional outer layer. J Adv Nurs 2007; 59(5): 520-29.
49.Brindle CT. Identifying high-risk ICU patients: use of an
absorbent soft silicone self-adherent bordered foam dressing
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50.Defloor T. The effect of position and mattress on interface
pressure. Appl Nurs Res 2000; 13(1): 2-11.
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Microclimate in context
M Clark, M Romanelli, SI Reger, VK Ranganathan, J Black, C Dealey
Introduction
Numerous factors have been implicated in the
aetiology and pathophysiology of pressure
ulcers1-3. Even so, it is clear that there is
much still to be learned about the complex
interactions between the many intrinsic and
extrinsic factors involved. Recently, interest
has been building in how modifying the
environment at or near the skin surface – the
microclimate – may affect risk of pressure ulcer
development4,5.
This paper defines the main parameters
involved in current understanding of
microclimate and explores what is known
about the relationship between microclimate
and pressure ulcer development. It also
describes interventions that may beneficially
alter microclimate. Discussion includes
the effect of different support surfaces on
microclimate and how management of
microclimate may help to avoid pressure
ulcers.
Fact File
In the context of pressure
ulcers, microclimate
usually refers to skin
temperature and moisture
conditions at the skin–
support surface interface.
What is microclimate?
In 1976, Roaf reported that the first UK-based
conference on pressure ulcers highlighted
known contributory factors to pressure ulcer
development: "We know how to avoid bed
sores and tissue necrosis – maintain the
circulation, avoid long continued pressure,
abrasions, extremes of heat and cold, maintain
a favourable micro-climate, avoid irritating
fluids and infection"6.
The maintenance of a favourable
microclimate was seen in early pressure ulcer
publications to be a key modifier of
the ability of skin and underlying soft tissue
to withstand prolonged stress, ie pressure
and shear. The important role of
microclimate modification in the prevention
of pressure ulcers has largely been overlooked
since the 1970s, but is now regaining
attention.
Microclimate was suggested by Roaf to
include skin temperature, humidity and air
movement6. However, today, the use of the
term microclimate in relation to pressure ulcers
usually refers to:
■■ skin surface or tissue temperature
and
■■ humidity or skin surface moisture at the
body–support surface interface2,7.
As described later, some support surfaces
use air movement to influence temperature and
humidity/moisture at the interface between skin
and the support surface.
Studies examining the effects of elements
of microclimate on skin and pressure ulcer
development are inconsistent in the definitions
used, making study interpretation and
comparison difficult. Some of the definitions
that have been used are discussed below.
Skin surface temperature
Methods used to measure skin surface
temperature include:
■■ measurement at 'radiative equilibrium' – ie
when the temperature of exposed skin has
reached steady state following exposure to
air
■■ measurement at the skin–support surface
interface with the patient still in contact with
the surface or very soon after moving out of
contact with the surface.
The first method – measurement at radiative
equilibrium – provides an indication of the
'intrinsic' skin (but not core body) temperature
of the patient (although still subject to external
variables such as ambient temperature). The
second method provides an indication of
the temperature at the skin–support surface
interface.
Temperature may be measured directly,
eg with a thermometer, or indirectly by using
infrared thermal imaging (thermography)8.
Humidity
Within the literature relating to microclimate,
'humidity' and 'skin moisture' are sometimes
used synonymously. However, strictly speaking
humidity relates to the amount of water vapour
in the air:
■■ absolute humidity – is expressed as the
weight of water in grams per cubic metre of
air (g/m3)
■■ relative humidity (often abbreviated
to humidity) – is a ratio expressed as a
percentage that relates the amount of water
vapour in the air at a specific air temperature
to the maximum amount of water vapour
that body of air would hold at that
temperature (Box 1). The relative humidity
of the general surroundings is known as
ambient humidity.
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BOX 1 Definitions of humidity
Absolute
humidity (g/m3)
= weight of water vapour
volume of air
Relative humidity
at a specific
temperature (%)
= amount of water vapour in the air at a specific
temperature
maximum amount of water vapour that can be held in
the air at that temperature
Fact File
●● Definitions of each
element of microclimate
require further
clarification; the
terminology around skin
moisture and humidity
can be particularly
confusing.
●● Raised skin temperature
may be related to
pressure ulceration by
increasing susceptibility
to the ischaemic
effects of pressure and
shear stresses, and by
weakening the stratum
corneum.
Absolute humidity is affected by air
temperature: warmer air is able to hold more
water vapour than cooler air. Therefore, for the
same absolute humidity, warmer air will have a
lower relative humidity than cooler air.
Relative humidity is measured using a
device known as a hygrometer. In relation to
skin, relative humidity may be measured at
the interface between the skin and a support
surface, or just above exposed skin9,10.
Skin moisture
Skin moisture is difficult to define: it may refer
to the presence of fluid on the skin surface
('wetness') from perspiration, incontinence
or wound/fistula drainage, or to the moisture
content of the outermost layer of the skin itself
(the stratum corneum).
Skin moisture can be assessed
subjectively, eg using the moisture subscale
of the Braden scale for assessing risk of
pressure ulceration: this classifies skin as
dry or having some degree of moisture as
indicated by frequency of linen changes
and detection of dampness on the skin
surface11. Methods to quantitatively assess
the moisture content of the stratum corneum
include measurement of electrical properties
such as skin surface conductance or
capacitance 12.
Air movement
Air movement is the least investigated factor
of Roaf's original definition of microclimate,
but is used by some support surfaces to aid
microclimate control by modifying temperature
and humidity/skin moisture. The flow of air
can be expressed quantitatively as the velocity
(speed) of airflow across the skin, eg in metres
per second, or by the rate at which air is
pumped through a support surface, eg in litres
per minute.
How is skin surface temperature
related to pressure ulcer risk?
Raised body temperature (pyrexia) is a recognised
risk factor for pressure ulcers13,14. It is well
established that increasing body temperature
by 1°C raises the metabolic activity (ie the need
for oxygen and energy) of body tissues by about
10%15. By definition, ischaemia occurs when tissue
perfusion is not sufficient to meet the needs of
the tissue. Therefore, when metabolic needs are
raised, a smaller reduction in tissue perfusion will
produce ischaemia than when metabolic needs
are steady. This suggests that in a patient with
elevated body temperature and compromised
tissue perfusion due to exposure to pressure
and shear, ischaemia and tissue damage may
occur more quickly and at lower levels and/or
shorter durations of pressure/shear than if body
temperature was normal16.
This concept has been extended to suggest
that increased skin temperature may play a role
in the development of pressure ulcers.
In addition, temperature affects the strength
of the stratum corneum: at 35°C the mechanical
strength of the stratum corneum is 25% of that
at 30°C17.
In contrast, low core body temperature
during surgery is associated with pressure ulcer
development14. To examine whether preventing
hypothermia during surgery would reduce the
incidence of pressure ulcers, Scott et al provided
forced air warming therapy during surgery
to 338 patients. There was an absolute risk
reduction in pressure ulcer incidence of 4.8%
and a relative risk reduction of 46% between
those who received warming and those who
received standard care. However, this difference
did not achieve statistical significance18.
What affects skin temperature?
It seems intuitive that raised core body
temperature would correlate with increased skin
temperature, and that this would perhaps help to
explain why pyrexia is a risk factor for pressure
ulcers. However, clear evidence of a correlation
is lacking and one small study found a negative
correlation between these parameters19.
Other factors that may increase skin
temperature include high ambient temperature,
high ambient humidity, low exposure to air,
and contact with another surface (eg clothing,
support surfaces, dressings and incontinence
pads).
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Fact File
●● Skin temperature
is highly variable
and influenced by
a very wide range
of environmental,
physiological and
pathological factors,
including ambient
humidity and
temperature and
disease processes.
●● Further research is
required to establish
whether skin
temperature can be
used to determine
risk of or predict
imminent pressure ulcer
development.
●● Animal models have
suggested that skin
cooling may protect
tissues against the
effects of pressure.
However, the
association between
intraoperative
hypothermia and
pressure ulcers
suggests that there
may come a point
where cooling-induced
vasoconstriction may
exacerbate pressureinduced ischaemia.
The skin has a major role in regulating
body temperature. The two main mechanisms
involved in cooling are:
■■ dermal vasodilatation – which increases
skin blood flow and causes heat loss by
convection and conduction
■■ sweating – perspiration cools the skin
through evaporation.
These responses may be triggered by
increases in core body temperature, eg
during pyrexial illness or exertion, increases
in ambient temperature, or covering the skin
with clothing or a support surface. Local
perspiration increases considerably when the
skin is warmed above about 33°C20. Perspiration
may also be triggered in conditions such as
shock, hyperthyroidism, and hypoglycaemia.
When ambient humidity is high, evaporation of
perspiration may be slowed causing perspiration
to accumulate on the skin.
Increased perspiration is particularly relevant
to pressure ulcer risk because moisture on the
skin surface can reduce the skin's resilience
and increase the coefficient of friction of skin,
making it more prone to pressure, shear stresses
and friction (see: Pressure in context21, pages 2–10
and Shear and friction in context22, pages 11–18).
Conversely, the skin's contribution to
conservation of body heat is largely mediated by
dermal vasoconstriction.
What is normal skin temperature?
Surprisingly, there is limited information on
normal skin temperature over anatomical sites
prone to pressure ulcer development. One key
study proposed that sites prone to pressure
ulcer development were cooler than adjacent
body sites23. However, there were several
weaknesses in this study; for example, ambient
room temperature was unreported, as was the
duration for which the skin was exposed to room
temperature prior to temperature measurement.
Can skin surface temperature predict pressure
ulcer development?
Several studies have investigated skin
temperature associated with early (Category/
Stage 1) pressure damage. These found
inconsistent changes in skin temperature of
pressure damaged areas: it could be increased
(possibly as a result of inflammation), the same,
or decreased (possibly as a result of ischaemia)
in comparison with temperature at undamaged
areas24,25.
The few studies that have examined whether
skin temperature can predict pressure ulceration
have been inconclusive. In a prospective cohort
study, Clark measured the sacral skin temperature
of 52 elderly hospital patients9. Of this cohort,
six developed pressure ulcers; however, the skin
temperature of the patients who did and did not
develop pressure ulcers was similar. This study was
confounded by a non-uniform allocation of support
surfaces to the recruited subjects9. However,
one small study of neurologically impaired
patients found that sacral skin temperature may
increase 24–96 hours before sacral pressure ulcer
development by at least 1.2°C26.
A recent study has examined whether skin
temperature regulation may predict pressure ulcer
development27. A small sample of nursing home
patients wore skin temperature monitors taped
to the right mid-axillary line continuously for five
days. The study found that patients at high risk
or who went on to develop pressure ulcers had
least variability in skin temperature, suggesting
impaired skin temperature regulation27. However,
it is unknown whether reduced ability to regulate
skin temperature is directly related to pressure
ulcer development or if it is a general marker of
declining physiological condition.
How does changing local skin temperature
affect risk of pressure ulcer development?
Some investigators have examined how
changing local skin temperature affects the
impact of pressure on tissues. In an animal
study, a known pressure (100mmHg) was
applied for five hours with indentors heated to
25, 35, 40 or 45°C28. Moderate muscle damage
was seen at 35°C and cutaneous and deep
tissue damage were observed at 40 and 45°C
(note that there may have been an element of
thermal damage at 45°C)28. No cutaneous or
muscle damage was observed where load was
applied at 25°C, suggesting that local cooling
may have a protective effect.
More recently, Lachenbruch has argued
from prior studies (including that of Kokate
et al28) that a 5°C reduction in skin–support
surface interface temperature would confer
tissue protective effects similar in magnitude
to the interface pressure reductions afforded
by the most expensive support surfaces20. This
hypothesis remains untested.
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Although cooling may provide some
protective effects, as mentioned previously
hypothermia during surgery may contribute
to the development of postoperative pressure
ulcers17.
Figure 1 Incontinenceassociated dermatitis
(courtesy of J Black)
Fact File
●● Excessive skin moisture
and high relative
humidity weaken
skin and increase the
coefficient of friction
of skin, increasing the
likelihood of damage
from pressure, shear
and friction.
●● Dry skin is weakened
and more vulnerable to
damage, eg by pressure,
shear stresses and
friction.
●● Investigations into the
effects of air movement
need to take place
to confirm or refute
whether this aspect
of microclimate is
significant in pressure
ulcer aetiology.
●● Until therapeutic ranges
for temperature and
humidity/skin moisture
at the patient–support
surface interface are
identified, clinical
judgement should be
exercised to avoid
extremes (high or low)
in these factors.
How do humidity and skin moisture
relate to pressure ulcer risk?
Increased skin moisture, especially when due
to incontinence, has long been recognised
as an important risk factor for pressure ulcer
development29-31. However, there is limited
quantitative data on skin moisture or humidity
to support this view.
Clark reported that the humidity just above
the sacral skin of elderly hospital patients who
subsequently developed Category/Stage II
pressure ulcers was higher than the humidity of
patients who did not9.
Increased skin moisture as measured by
electrical capacitance has been found in a
study in Indonesia and in a small pilot study
to correlate with the development of pressure
ulcers32,33. However, further studies are required
to determine whether measuring skin moisture
in this way may prove useful in identifying
patients who would benefit from additional
intervention to prevent pressure ulceration.
Effects of excessive skin moisture
Excessive moisture on the skin surface, eg
as a result of perspiration, urinary or faecal
incontinence, wound/fistula drainage or vomit,
is thought to contribute to increased risk for
the development of pressure ulceration by
weakening skin. Moisture can weaken the
crosslinks between the collagen in the dermis
and soften the stratum corneum34. This can
cause maceration (or incontinence-associated
dermatitis if the liquid involved is urine – Figure
1) and also increases the exposure of underlying
blood vessels to the effects of pressure and
shear stresses.
In addition, excessive moisture can
significantly increase the skin's coefficient of
friction35, leading to increased likelihood of skin
damage from friction and shear stresses (see:
Shear and friction in context22, pages 11–18).
Relative humidity also affects the strength of
the stratum corneum: at a relative humidity of
100% the stratum corneum is 25 times weaker
than at 50% relative humidity16.
Effects of excessive skin dryness
Ageing skin is less resilient and more vulnerable
to damage than is younger skin because it is
generally thinner, structurally weaker and drier36.
Dry skin has reduced lipid levels, water content,
tensile strength, flexibility and junctional
integrity between the dermis and the epidermis.
Low ambient humidity reduces water content
in the stratum corneum12. In the USA, the
Agency for Health Care Policy and Research
guidelines on the prevention of pressure ulcers,
recommends avoiding ambient relative humidity
below 40% to reduce the likelihood of dry skin37.
How does air movement relate to
pressure ulcer development?
There appears to have been no research to look
specifically at the possible role of air movement
in the aetiology of pressure ulcers. The relevance
of air movement may relate to its potential to
affect skin temperature and moisture content
through convection and evaporation.
What don't we know about
microclimate as a cause of pressure
ulcers?
The body of literature linking pressure ulcers
and microclimate is relatively small, with
little characterisation of interactions between
skin and fabric (eg support surface covers).
Furthermore, there is evidence of wide intra- and
inter-individual differences in skin microclimate
parameters, but the effect of these on pressure
ulcer development is unclear. Interpretation of
available data is therefore challenging.
The in vivo experimental studies on interactions
between skin and fabrics that have been
performed have rarely led to any significant
results or definitive conclusions38. This may be
partly explained by the considerable differences
that may exist in skin condition (eg hydration,
surface roughness, adhesion between skin layers)
between individuals and between different
anatomical locations in the same individual38.
Clinical management of
microclimate
The needs of the patient should be carefully
assessed before modifications in temperature
and humidity/skin moisture are undertaken.
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A key strategy in the management of
microclimate is control of the underlying
cause of the extreme of temperature or skin
moisture, eg pyrexia or incontinence. Patients
who are hot may be cooled using simple
measures such as reduction in the number of
covers, avoidance of plastic mattress coverings,
frequent repositioning, use of a fan and wearing
breathable cotton clothing. Where available
in climates with high ambient humidity, air
conditioning may be helpful in cooling and
reducing humidity.
Repositioning
The importance of the role of repositioning
in controlling microclimate should not be
underestimated. Some mattress covers are made
of material that prevents dissipation of heat.
Repositioning patients allows skin that has been
in contact with the mattress cover to be exposed
to air and to become cooler. It also provides an
opportunity for perspiration to evaporate.
Fact File
Management of
microclimate is one
component of pressure
ulcer prevention and
needs to take place
within the context of a
comprehensive pressure
ulcer prevention protocol
that takes into account
patient comfort.
Figure 2 Candidal infection
in skin fold of a bariatric
patient (courtesy of J Black)
Skin care
Barrier creams and sprays can be useful in
protecting moist skin from further damage,
especially from urine2,39. However, it is best to
manage incontinence where possible so that the
skin does not come into contact with urine in
the first place.
For patients who are incontinent and
require the use of absorbent underpads, use of
breathable pads which allow transmission of
moisture vapour is preferable. Care is required
to ensure that the use of underpads does not
interfere with the pressure redistribution or
microclimate management properties of any
support surface in use.
Bariatric patients who are prone to excessive
perspiration may benefit from frequent washing
and changing of clothes and bed linen to control
skin moisture. Accumulation of moisture in
the skin folds of bariatric patients may be a
particular problem, and result in intertriginous
dermatitis with bacterial and candidal infections
(Figure 2).
The use of emollients can assist in
ameliorating dry skin and may reduce the risk of
skin damage2. They should be applied liberally
and frequently (eg up to three to four times
daily) when the skin is very dry, and following
washing or bathing when they will help to trap
water onto the skin.
Role of support surfaces in managing
microclimate
Any surface that comes into contact with
skin has the potential to alter microclimate by
changing the rate of evaporation of moisture and
the rate at which heat dissipates from the skin.
The overall effect on microclimate is dependent
on numerous factors, including the nature of
the support surface itself (ie what is made from,
how the material is conformed, what sort of
cover it has)15,40.
For example, foam surfaces tend to increase
skin temperature because they have poor
heat transfer properties15. The effect of foam
products on moisture depends on the porosity
of the cover15. Gel filled products may initially
have a cooling effect that wears off after more
than two hours of patient contact and tend
to increase humidity at the skin surface15.
Fluid filled products that utilise high heat
capacity liquids have the potential to reduce
skin temperature15. Alternating pressure
air mattresses may limit skin temperature
increases41.
Some specialised support surfaces for beds
have features that aid active management of
microclimate by allowing air to flow through
their surfaces, for example low air loss features
or air fluidised beds. The air flow cools skin
through convection and the evaporation of
moisture from the skin surface42.
Low air loss surfaces
Low air loss surfaces pump air into a series
of cushions and then allow the air to escape
through small holes (porosities) in the cushions'
covers. The air flows along the inside of a
Water vapour
Vapour permeable
cover – water
vapour is drawn
through by the flow
of air on the other
side of the cover
Low air loss cushions
Figure 3 Mode of action of low air loss surfaces
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Figure 4 Mode of action of
air fluidised support surfaces
Porous cover that allows
air to pass out and fluids
to pass through
Silicone beads
suspended in air flow
Warm
compressed air
vapour permeable patient contact layer drawing
moisture and heat through the contact layer
and away from the skin16 (Figure 3). Low air
loss surfaces have been shown to lower skin
temperature and to produce lower moisture gain
than standard hospital mattresses43.
Air fluidised support surfaces
Air fluidised support surfaces comprise solid
silicone particles the size of sand through which
air is forced. The air flow causes the particles to
take on properties of a liquid. The cover over the
particles is porous allowing air to escape and body
fluids (eg sweat, urine) to flow through (Figure 4).
Air fluidised beds are considered to be the most
drying support surface; the fluid loss increases
linearly with increased air flow temperature44.
The air flowing through low air loss and air
fluidised devices is generally warmed in the
range of approximately 28–35°C and can be
adjusted. This facility is undeniably useful, but
has to be used with considerable care to prevent
inappropriate cooling or heating.
Fact File
●● Low air loss and air
fluidised support
systems provide
mechanisms for active
microclimate control.
●● In the absence of clinical
evidence, choice of
support surface for
the management of
microclimate remains
reliant on clinical
judgement.
●● Further research is
required to evaluate
the effectiveness of
microclimate control
features in preventing
pressure ulcers.
Choosing a support surface to manage
microclimate
Despite the availability of several forms of low air
loss and air fluidised support systems, there is little
information to guide decisions about which surface
to use for which patient. Choice of support surface
will be guided by clinical judgement and take into
account numerous factors including the patient's
need for pressure redistribution, the patient's size,
ability to turn or move independently and body
temperature, the presence of moisture on the skin
or concomitant conditions such as incontinence.
(See: Pressure in context21, pages 2–10, for further
information on pressure redistributing support
surfaces.)
Whilst air loss systems may be helpful in
keeping immobile patients cool and dry, it is
important to recognise that patients must still
be turned and repositioned on these devices.
According to patient needs, the frequency of
positioning may be reduced in comparison with
standard mattresses (see: Pressure in context21,
pages 2–10).
Recent research has highlighted the
importance of minimising layers of bedding
between patients and low air loss support
surfaces to prevent skin temperature rises45.
Impact of microclimate management on
pressure ulcer prevention
Support surfaces designed to aid microclimate
management also provide pressure
redistribution. This complicates assessment
of the impact of microclimate management
on incidence of pressure ulcers, and evidence
demonstrating that management of microclimate
directly prevents pressure ulcers is currently
lacking.
Even so, clinical studies have shown that
some advanced support surfaces that affect skin
temperature and moisture, eg air fluidised and
low air loss surfaces, are more effective than
standard foam mattresses for the treatment
of pressure ulcers46. In addition, there is some
evidence that low air loss beds reduce the
incidence of pressure ulcers in intensive care47.
Conclusion
The concept of microclimate in relation to pressure
ulcers has existed for some time. However,
microclimate and its elements remain to be fully
defined, and its relationship to pressure ulcer
development clearly characterised. Evidence to
date suggests that extremes of skin temperature
and/or humidity/skin moisture appear to increase
the sensitivity of skin to the damaging effects of
pressure, shear stresses and friction.
This suggests, therefore, that the overall aim
of microclimate management should be to avoid
extremes of temperature or skin moisture and
to enhance patient comfort. However, further
investigation is needed to establish the effects
of 'traditional' preventive interventions (such
as repositioning) and those of support surfaces
on elements of skin microclimate and pressure
ulcer incidence. Low air loss support surfaces
and air fluidised beds are designed to assist with
microclimate management, but in the absence of
evidence defining optimal skin temperature and
moisture levels, clinical judgement is required for
effective and safe use.
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KCI is Your Partner in
Pressure Ulcer Prevention
With more than 20 years of skin management expertise, KCI can help your facility
improve its pressure ulcer performance. In addition to our family of Therapeutic
Support Systems, KCI offers comprehensive programs designed to manage your pressure
ulcer prevention needs. With the KCI Wound Care Program and our robust prevalence
and incidence database, we’re with you every step of the way to achieve improved,
measurable pressure ulcer outcomes.
For more information about KCI prevalence and incidence programs, contact:
KCI U.S.
www.kci1.com
KCI International
www.kci-medical.com
©2008, KCI Licensing, Inc. All Rights Reserved. All trademarks designated herein are property of KCI, its affiliates and licensors. Those KCI trademarks designated
with the “®” or “TM” symbol are registered in at least one country where this product/work is commercialized, but not necessarily in all such countries. Most KCI
products referenced herein are subject to patents and pending patents.
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